期刊
BLOOD
卷 110, 期 3, 页码 986-993出版社
AMER SOC HEMATOLOGY
DOI: 10.1182/blood-2006-12-064626
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- NCI NIH HHS [1P01 CA 108671, P01 CA108671] Funding Source: Medline
In order to investigate the biologic processes underlying and resulting from the megalkaryocytic hyperplasia that characterizes idiopathic myelofibrosis (IMF), peripheral blood CD34(+) cells isolated from patients with IMF, polycythemia vera (PV), and G-CSF-mobilized healthy volunteers were cultured in the presence of stem cell factor and thrombopoietin. IMF CD34(+) cells generated 24-fold greater numbers of megakaryocytes (MKs) than normal CD34(+) cells. IMF MKs were also shown to have a delayed pattern of apoptosis and to overexpress the antiapoptotic protein bcl-xL. MK hyperplasia in IMF is, therefore, likely a consequence of both the increased ability of IMF progenitor cells to generate MKs and a decreased rate of MK apoptosis. Media conditioned (CM) by CD61(+) cells generated in vitro from CD34(+) cells were then assayed for the levels of growth factors and proteases. Higher levels of transforming growth factor-beta (TGF-beta) and active matrix metalloprotein-ase-9 (MMP9) were observed in media conditioned with IMF CD61(+) cells than normal or PV CD61(+) cells. Both normal and IMF CD61(+) cells produced similar levels of VEGF. MK-derived TGF-B and MMP-9, therefore, likely contribute to the development of many pathological epiphenomena associated with IMF.
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